AIM: To investigate the effects of allicin on both telomeraseactivity and apoptosis in gastric cancer SGC-7901 cells.METHODS: The gastric cancer SGC-7901 adenocarcinomacells were treated with allicin and the cell cycl...AIM: To investigate the effects of allicin on both telomeraseactivity and apoptosis in gastric cancer SGC-7901 cells.METHODS: The gastric cancer SGC-7901 adenocarcinomacells were treated with allicin and the cell cycle, inhibitoryrate, apoptosis, telomerase activity and morphologic changeswere studied by MTT assay, flow cytometry (FCM), TRAP-PCR-ELISA assay, light microscope, electron microscoperespectively. Results were compared with that of AZT (3′-Azido-3′-deoxythymidine).RESULTS: SGC-7901 cells were suppressed after exposureto allicin of 0.016 mg/ml, 0.05 mg/ml, and 0.1 mg/mi for48 h. Compared with the control, the difference wassignificant (P＜0.05). Allicin could induce apoptosis of thecells in a dose-dependent and non-linear manner andincrease the proportion of cells in the G2/M phase. Comparedwith the control, the difference was significant in terms ofthe percentage of cells in the G2/M phase (P＜0.05). Allicincould inhibit telomerase activity in a time-dependent anddose-dependent pattern. After exposure to allicin at 0.016mg/ml for 24 hours, SGC-7901 cells showed typicalmorphologic change.CONCLUSION: Allicin can inhibit telomerase activity andinduce apoptosis of gastric cancer SGC-7901 cells. Allicinmay be more effective than AZT.展开更多
AIM:To investigate the effects of growth inhibition ofhuman gastric cancer SGC-7901 cell with RRR-α-tocopherylsuccinate(VES),a derivative of natural Vitamin E,viainducing apoptosis and DNA synthesis arrest.METHODS:Hu...AIM:To investigate the effects of growth inhibition ofhuman gastric cancer SGC-7901 cell with RRR-α-tocopherylsuccinate(VES),a derivative of natural Vitamin E,viainducing apoptosis and DNA synthesis arrest.METHODS:Human gastric cancer SGC-7901 cells wereregularly incubated in the presence of VES at 5,10 and20mg.L^(-1)(VES was dissolved in absolute ethanol anddiluted in RPMI 1640 complete condition mediacorrespondingly to a final concentration of VES and lmL.L^(-1)ethanol),succinic acid and ethanol equivalents asvehicle(VEH)control and condition-media only asuntreated(UT)control.Trypan blue dye exclusionanalysis and MTT assay were applied to detect the cellproliferation.37kBq of tritiated thymidine was added tocells and [~3H]TdR uptake was measured to observe DNAsynthesis.Apoptotic morphology was observed byelectron microscopy and DAPI staining.Flow cytometryand terminal deoxynucleotidyl transferase-mediated dUTPnick end labeling(TUNEL)assay were performed to detectVES-triggered apoptosis.RESULTS:VES inhibited SGC-7901 cell growth in a dose-dependent manner.The growth curve showed suppressionby 24.7%,49.2% and 68.7% following 24h of VEStreatment at 5,10 and 20 mg·L^(-1),respectively,similar tothe findings from MTT assay.DNA synthesis wasevidently reduced by 35%,45% and 98% after 24h VEStreatment at 20 mg·L^(-1)and 48h at 10 and 20 mg·L^(-1),respectively.VES induced SGC-7901 cells to undergoapoptosis with typically apoptotic characteristics,including morphological changes of.chromatincondensation,chromatincrescent formation/margination,nucleus fragmentation and apoptotic body formation,typical apoptotic sub-G1 peak by flow cytometry andincrease of apoptotic cells by TUNEL assay in which 90%of cells underwent apoptosis after 48h of VES treatment at20 mg·L^(-1).CONCLUSION:VES can inhibit human gastric cancer SGC-7901 cell growth by inducing apoptosis and DNA synthesisarrest,inhibition of SGC-7901 cell growth by VES is dose-and time-dependent.Therefore VES can function as apotent chemotherapeutic agent against hu展开更多
基金the Natural Science Foundation of Jiangsu,Province No.BJ98110
文摘AIM: To investigate the effects of allicin on both telomeraseactivity and apoptosis in gastric cancer SGC-7901 cells.METHODS: The gastric cancer SGC-7901 adenocarcinomacells were treated with allicin and the cell cycle, inhibitoryrate, apoptosis, telomerase activity and morphologic changeswere studied by MTT assay, flow cytometry (FCM), TRAP-PCR-ELISA assay, light microscope, electron microscoperespectively. Results were compared with that of AZT (3′-Azido-3′-deoxythymidine).RESULTS: SGC-7901 cells were suppressed after exposureto allicin of 0.016 mg/ml, 0.05 mg/ml, and 0.1 mg/mi for48 h. Compared with the control, the difference wassignificant (P＜0.05). Allicin could induce apoptosis of thecells in a dose-dependent and non-linear manner andincrease the proportion of cells in the G2/M phase. Comparedwith the control, the difference was significant in terms ofthe percentage of cells in the G2/M phase (P＜0.05). Allicincould inhibit telomerase activity in a time-dependent anddose-dependent pattern. After exposure to allicin at 0.016mg/ml for 24 hours, SGC-7901 cells showed typicalmorphologic change.CONCLUSION: Allicin can inhibit telomerase activity andinduce apoptosis of gastric cancer SGC-7901 cells. Allicinmay be more effective than AZT.
基金National Natural Science Foundation of China,No.39870662
文摘AIM:To investigate the effects of growth inhibition ofhuman gastric cancer SGC-7901 cell with RRR-α-tocopherylsuccinate(VES),a derivative of natural Vitamin E,viainducing apoptosis and DNA synthesis arrest.METHODS:Human gastric cancer SGC-7901 cells wereregularly incubated in the presence of VES at 5,10 and20mg.L^(-1)(VES was dissolved in absolute ethanol anddiluted in RPMI 1640 complete condition mediacorrespondingly to a final concentration of VES and lmL.L^(-1)ethanol),succinic acid and ethanol equivalents asvehicle(VEH)control and condition-media only asuntreated(UT)control.Trypan blue dye exclusionanalysis and MTT assay were applied to detect the cellproliferation.37kBq of tritiated thymidine was added tocells and [~3H]TdR uptake was measured to observe DNAsynthesis.Apoptotic morphology was observed byelectron microscopy and DAPI staining.Flow cytometryand terminal deoxynucleotidyl transferase-mediated dUTPnick end labeling(TUNEL)assay were performed to detectVES-triggered apoptosis.RESULTS:VES inhibited SGC-7901 cell growth in a dose-dependent manner.The growth curve showed suppressionby 24.7%,49.2% and 68.7% following 24h of VEStreatment at 5,10 and 20 mg·L^(-1),respectively,similar tothe findings from MTT assay.DNA synthesis wasevidently reduced by 35%,45% and 98% after 24h VEStreatment at 20 mg·L^(-1)and 48h at 10 and 20 mg·L^(-1),respectively.VES induced SGC-7901 cells to undergoapoptosis with typically apoptotic characteristics,including morphological changes of.chromatincondensation,chromatincrescent formation/margination,nucleus fragmentation and apoptotic body formation,typical apoptotic sub-G1 peak by flow cytometry andincrease of apoptotic cells by TUNEL assay in which 90%of cells underwent apoptosis after 48h of VES treatment at20 mg·L^(-1).CONCLUSION:VES can inhibit human gastric cancer SGC-7901 cell growth by inducing apoptosis and DNA synthesisarrest,inhibition of SGC-7901 cell growth by VES is dose-and time-dependent.Therefore VES can function as apotent chemotherapeutic agent against hu
